To properly protect a herd or flock of animals from bacterial and viral infections, it is important that the animals maintain a level of immunity against a pathogen at the point when effective passive immunity from circulating maternal antibodies is lost. In mammals, a fetus receives maternally-synthesized antibodies while in utero which confers passive protection to the fetus. In the avian species, immunity is transferred from the hen via the egg, and the progeny in the first few months of life are protected against toxins, viruses and pathogenic bacteria. The levels of these maternal antibodies gradually decline as the newborn begins to synthesize its own antibodies.
The first exposure of an animal to a particular immunogen triggers a priming response. After initial contact with an immunogen, there is a latent period before antibody to that immunogen is detectable in the serum, generally about 1-2 weeks, during which time T and B cells make contact with the immunogen, proliferate, differentiate, and secrete antibody which then increases exponentially in the serum of the animal, reaches a steady state and then, as the immune response shuts down, decreases in concentration in the serum. This priming contact with an immunogen leaves the immunized animal with a cellular memory of the contact such that, upon a second, later contact with the immunogen, a secondary or anamnestic (memory) immune response is automatically triggered in which the lag phase is considerably shorter and the antibody appears much faster and at a higher concentration in the serum. This capacity to make a secondary response provides an advantage to an animal that survives the first contact with an invading pathogen.
Maternal antibody, while capable of providing passive protection to the neonate against a variety of infectious agents or their toxins, may also interfere with the animal's active response to an immunogen by reacting with and tying up the immunogen. As a result, administration of a priming dose of an immunogen to stimulate active immunity in the newborn must be delayed until the level of circulating maternal antibodies has decreased.
To provide continuous coverage so that immunity is maintained after the disappearance of maternal antibodies, the herd may be immunized en masse when all animals have lost passive immunity. A drawback of this approach is that there will be a certain percentage of animals who lose immunity before the rest of the group and are therefore vulnerable during the interim. Another approach is to vaccinate an animal with an immunogen repeatedly from day one until they are found capable of responding, but the stress on the animal and expense for the breeder prohibits this tactic. Yet another approach is to administer to a young animal, a priming dose of an immunogen in a preparation that will present the immunogen in a slowly dissipating material. Examples of such preparations are an injectable water-in-oil emulsion containing live virus, a suspension of an antigen in Freund's complete adjuvant or phosphatidylcholine (egg-lecithin)- or cholesterol-based liposomes containing an entrapped immunogen. However, such preparations do not provide adequate long-term delivery of an immunogen and may cause adverse reactions such as granuloma formation. There is also the risk of the person administering the injection accidentally injecting themselves with the preparation, resulting in an adverse reaction from the injected ingredients. For example, injecting mineral oil into a human finger, or other tissue or body part, will cause severe reaction and may result in the loss of tissue or worse.
Therefore, it is an object of the invention to provide an effective method for priming the immune system of a young animal to achieve a virtually immediate active immune response to infection by a pathogenic organism at the point where such protection is no longer provided by maternal antibodies, without irritation or undue stress caused to the animal. Another object is to provide an effective method for immunizing a large number of animals.